Cytotoxic T cell

About: Cytotoxic T cell is a research topic. Over the lifetime, 92492 publications have been published within this topic receiving 4768477 citations. The topic is also known as: killer T cell & cytotoxic T lymphocyte.

HTLV-I basic leucine zipper factor gene mRNA supports proliferation of adult T cell leukemia cells

Abstract: Human T cell leukemia virus type I (HTLV-I) causes adult T cell leukemia (ATL) in 2–5% of carriers after a long latent period. An HTLV-I encoded protein, Tax, induces proliferation and inhibits apoptosis, resulting in clonal proliferation of infected cells. However, tax gene expression in ATL cells is disrupted by several mechanisms, including genetic changes in the tax gene and DNA methylation/deletion of the 5′ long terminal repeat (LTR). Because Tax is the major target of cytotoxic T-lymphocytes in vivo, loss of Tax expression should enable ATL cells to escape the host immune system. The 5′ LTR of HTLV-I is frequently hypermethylated or deleted in ATL cells, whereas the 3′ LTR remains unmethylated and intact, suggesting the involvement of the 3′ LTR in leukemogenesis. Here we show that a gene encoded by the minus strand of the HTLV-I proviral genome, HTLV-I basic leucine zipper factor (HBZ), is transcribed from 3′-LTR in all ATL cells. Suppression of HBZ gene transcription by short interfering RNA inhibits proliferation of ATL cells. In addition, HBZ gene expression promotes proliferation of a human T cell line. Analyses of T cell lines transfected with mutated HBZ genes showed that HBZ promotes T cell proliferation in its RNA form, whereas HBZ protein suppresses Tax-mediated viral transcription through the 5′ LTR. Thus, the single HBZ gene has bimodal functions in two different molecular forms. The growth-promoting activity of HBZ RNA likely plays an important role in oncogenesis by HTLV-I.

T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis

Abstract: Encounters with antigen can stimulate T cells to become activated and proliferate, become nonresponsive to antigen, or to die. T cell death was shown to be a physiological response to interleukin-2-stimulated cell cycling and T cell receptor reengagement at high antigen doses. This feedback regulatory mechanism attenuates the immune response by deleting a portion of newly dividing, antigen-reactive T cells. This mechanism deleted autoreactive T cells and abrogated the clinical and pathological signs of autoimmune encephalomyelitis in mice after repetitive administration of myelin basic protein.

Transfer of specific cytotoxic T lymphocytes protects mice inoculated with influenza virus

Abstract: THERE is remarkably little information about the possible importance of cell-mediated immune responses in the protection of hosts during influenza virus infection. It has recently been found that specific cytotoxic T cells (Tc) can be recovered from the spleens of mice previously inoculated intranasally or intravenously with live virus1–4 and peak activity occurs about 6 d after virus inoculation. Furthermore, Tc are found in the lungs and the lymph nodes draining the lungs of infected mice in conditions which suggest that these cells might be important in host recovery from this infection5. Adoptive transfer of primary or secondary immune spleen cells to mice inoculated intranasally with a lethal dose of A/WSN virus caused a significant reduction of infectious virus levels in the lungs and prevented death6. The active cells in the transferred population were T lymphocytes. This report shows that the protective effects conferred by the transferred T cells in these conditions are largely, if not entirely, due to Tc.